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Old 07-22-2005, 09:23 AM   #1
Bennett37
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Join Date: Jul 2003
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Early diastolic dysfunction?

I am a 39 year old male in good health. I am not overweight and exercise regularly. Last spring, my doc noticed a slight irregularity on an ekg. He suspected LVH so he sent me for an echo. The echo came back showing everything in the normal range except there was some equalization of the E to A wave which could be indicative of early diastolic dysfunction according to the cardio who read the report. Last fall I went to a cardio who examined me and read the report. He really didn't think there was a problem but had me do a stress test and looked at the echo tape. I did great on the stress test (the ekg was still a little off). He did see the E to A wave issue on the echo. He said let's redo it in 6 months or so.

Yesterday they redid the echo. It still show some equaliztion (70:60) with some slight reversals in one chamber. Everything else looked great. My bp is usually 115/68 or so. The tech said that she didn't think I had anything to worry about, but since I do worry, until I hear from the doc I am going to be concerned. I did read one article that stated that diastolic dysfunction would be extremly unlikely if there was no enlargement of the ventricular wall (mine are normal size).

Any input?
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Old 07-22-2005, 10:15 AM   #2
Lenin
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Re: Early diastolic dysfunction?

I think all is probably OK. It sounds like something worth monitoring long term though,

Here's a deep read on Cardiac Tamponade that you miight find engrossing...for HOURS perhaps. Provbably more info than anyone needs, though.

http://www.pifo.uvsq.fr/hebergement/webrea/index.php?option=com_content&task=view&i d=15&Itemid=69&lang=en

It seems to be a French govenment site so I'm sure it's OK to post the reference.
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Old 07-22-2005, 01:04 PM   #3
started04
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Re: Early diastolic dysfunction?

Bennentt37:

Unless this is apple to oranges is not clear. But an EKG displays of the heartbeat is the "P" wave (small blip) that is associated with the upper chambers, then the QRS complex (sharp spike) reflects the activity in the lower chamber, then "T" wave can be elevated, level or down (good for dx of MI and heart muscle damage, and then "U". For simplicity the waves are in alphabetical order. Verticle plane is in mvolts and horizontal plane is msec time on the graph...there is no E to A.

The dystole function would be shown with the Q beginning of the spike, R the peak, and S the bottom. Height of R would show the electrical charge, Q to S would be the time.

LVH (left ventricle hypertrophy) would be an enlargement when the heart is compensating for a system problem. I would agree a problem is unlikely if there are no compensating irregularities.
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Old 07-22-2005, 02:57 PM   #4
Lenin
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Re: Early diastolic dysfunction?

In a physiological setting, sudden reduction in ventricular dimensions at the start of systole creates pericardial depression which drives venous return, and the atria fill by anterograde systolic acceleration of the vena caval flow. The ventricle dilates on diastole and the ventricular depression thus created aspirates the blood of the atrium towards the ventricle (E-wave of rapid filling), but also from the vena cavae towards the atrium, inducing anterograde diastolic acceleration of caval flow. At end-diastole, atrial systole completes ventricular filling (A-wave).
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Old 07-23-2005, 05:32 PM   #5
started04
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Re: Early diastolic dysfunction?

[B]
Quote:
Originally Posted by Lenin
In a physiological setting, sudden reduction in ventricular dimensions at the start of systole creates pericardial depression which drives venous return, and the atria fill by anterograde systolic acceleration of the vena caval flow. The ventricle dilates on diastole and the ventricular depression thus created aspirates the blood of the atrium towards the ventricle (E-wave of rapid filling), but also from the vena cavae towards the atrium, inducing anterograde diastolic acceleration of caval flow. At end-diastole, atrial systole completes ventricular filling (A-wave).
What is the format of E-wave and A-wave? As stated in my prior post EKG wave forms are labeled "P" to "U" and deals with various segments (interval) and the relationship to their output to a vertical axis (Mv) and the co-relation to time expressed on the horizontal axis in msec. I don't know of any subset of E-A wave to the entire wave pattern displayed with an EKG.

For completeness the following:

Normal adult 12-lead ECG
The diagnosis of the normal electrocardiogram is made by excluding any recognised abnormality. It's description is therefore quite lengthy.
normal sinus rhythm
each P wave is followed by a QRS
P waves normal for the subject
P wave rate 60 - 100 bpm with <10% variation
rate <60 = sinus bradycardia
rate >100 = sinus tachycardia
variation >10% = sinus arrhythmia
normal QRS axis
normal P waves
height < 2.5 mm in lead II
width < 0.11 s in lead II
for abnormal P waves see right atrial hypertrophy, left atrial hypertrophy, atrial premature beat, hyperkalaemia (nothing about E-A wave!)
normal PR interval
0.12 to 0.20 s (3 - 5 small squares)
for short PR segment consider Wolff-Parkinson-White syndrome or Lown-Ganong-Levine syndrome (other causes - Duchenne muscular dystrophy, type II glycogen storage disease (Pompe's), HOCM)
for long PR interval see first degree heart block and 'trifasicular' block
normal QRS complex
< 0.12 s duration (3 small squares)
for abnormally wide QRS consider right or left bundle branch block, ventricular rhythm, hyperkalaemia, etc.
no pathological Q waves
no evidence of left or right ventricular hypertrophy
normal QT interval
Calculate the corrected QT interval (QTc) by dividing the QT interval by the square root of the preceeding R - R interval. Normal = 0.42 s.
Causes of long QT interval
myocardial infarction, myocarditis, diffuse myocardial disease
hypocalcaemia, hypothyrodism
subarachnoid haemorrhage, intracerebral haemorrhage
drugs (e.g. sotalol, amiodarone)
hereditary
Romano Ward syndrome (autosomal dominant)
Jervill + Lange Nielson syndrome (autosomal recessive) associated with sensorineural deafness
normal ST segment
no elevation or depression
causes of elevation include acute MI (e.g. anterior, inferior), left bundle branch block, normal variants (e.g. athletic heart, Edeiken pattern, high-take off), acute pericarditis
causes of depression include myocardial ischaemia, digoxin effect, ventricular hypertrophy, acute posterior MI, pulmonary embolus, left bundle branch block
normal T wave
causes of tall T waves include hyperkalaemia, hyperacute myocardial infarction and left bundle branch block
causes of small, flattened or inverted T waves are numerous and include ischaemia, age, race, hyperventilation, anxiety, drinking iced water, drugs, (e.g. digoxin), pericarditis, PE, intraventricular conduction delay (e.g. RBBB)and electrolyte disturbance.

Everything you wanted to know about EKG

Last edited by started04; 07-23-2005 at 05:41 PM.
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